Evidence map›Paper›PMID 27591120›Full record

ReviewMolecular and cellular endocrinology2017

Cellular senescence: Implications for metabolic disease.

Marissa J Schafer, Jordan D Miller, Nathan K LeBrasseur

Abstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 79 citations in OpenAlex.

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  10. The IGF System and Aging.Endocrine reviews · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Marissa J SchaferRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, 55905, USA; Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN, 55905, USA.
Jordan D MillerRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, 55905, USA; Department of Surgery, Mayo Clinic, Rochester, MN, 55905, USA; Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, 55905, USA.
Nathan K LeBrasseurRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, 55905, USA; Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN, 55905, USA. Electronic address: lebrasseur.nathan@mayo.edu.
Mayo Clinic in Arizona · USMayo Clinic · US

Funding

Systems Biology and Bioinformatics CoreP01AG041122 · NIA · MAYO CLINIC ROCHESTER · PI CAMPISI, JUDITH · 2012 to 2016
$9.8M
Effect of Aging on Preadipocyte DifferentiationR37AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 2016 to 2025
$6.6M
Effect of Aging on Preadipocyte DifferentiationR01AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 1997 to 2012
$3.7M
Therapeutic Strategy to slow progression of calcific aortic valve stenosisUH3TR000954 · NCATS · MAYO CLINIC ROCHESTER · PI ENRIQUEZ-SARANO, MAURICE, MILLER, JORDAN D · 2014 to 2015
$2.0M
Aging and Resiliency in Mice: Optimizing Assessment Protocols and Testing InterventionsR01AG053832 · NIA · MAYO CLINIC ROCHESTER · PI LEBRASSEUR, NATHAN K, MILLER, JORDAN D · 2016 to 2020
$2.0M
Role of SIRT6 in calcific aortic valve diseaseR01HL111121 · NHLBI · MAYO CLINIC ROCHESTER · PI MILLER, JORDAN D · 2013 to 2017
$2.0M
Therapeutic Strategy to slow progression of calcific aortic valve stenosisUH2TR000954 · NCATS · MAYO CLINIC ROCHESTER · PI ENRIQUEZ-SARANO, MAURICE, MILLER, JORDAN D · 2013 to 2014
$1.2M
Senescent Cell Transplantation ModelR21AG049182 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 2015 to 2016
$437k
NHLBI NIH HHS R01 HL111121NIA NIH HHS P01 AG041122NIA NIH HHS R01 AG013925NIA NIH HHS R01 AG053832NIA NIH HHS R21 AG049182
6 · The paper itself

Abstract

The growing burden of obesity- and aging-related diseases has hastened the search for governing biological processes. Cellular senescence is a stress-induced state of stable growth arrest strongly associated with aging that is aberrantly activated by obesity. The transition of a cell to a senescent state is demarcated by an array of phenotypic markers, and leveraging their context-dependent presentation is essential for determining the influence of senescent cells on tissue pathogenesis. Biomarkers of senescent cells have been identified in tissues that contribute to metabolic disease, including fat, liver, skeletal muscle, pancreata, and cardiovascular tissue, suggesting that pharmacological and behavioral interventions that alter their abundance and/or behavior may be a novel therapeutic strategy. However, contradictory findings with regard to a protective versus deleterious role of senescent cells in certain contexts emphasize the need for additional studies to uncover the complex interplay that defines multi-organ disease processes associated with obesity and aging.

Indexed as

Adipose TissueAgingAnimalsBiomarkersCell DeathCellular SenescenceDasatinibHumansLiverMetabolic DiseasesMuscle, SkeletalMyocardiumPancreasPhenotypeQuercetinBiomarkersDasatinibQuercetinAgingDiabetesExerciseInflammationObesitySenolytics

Identifiers

PMID27591120
PMCPMC5857952
OpenAlexW2515935238

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.